Pathologies of cardiogenic interest page Archivi - AF-ABLATION

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Coagulation disorders (combined deficiency of coagulation factors)
Hereditary combined coagulation factor deficiency is a congenital blood disorder caused by a variable reduction in the levels of coagulation factors II, VII, IX and X. The values ​​of natural anticoagulants, such as protein C, protein S, and protein Z, may also be decreased. The prevalence is unknown, but it is a relatively common disease. The bleeding symptoms can be mild or severe, begin in the neonatal period in severe cases, and often put the patient’s life at risk. They occur spontaneously or during surgery. Non-hematological symptoms are also often present, such as skeletal and developmental abnormalities (long dotted bones, shortening of the distal phalanges of the fingers, osteoporosis and skin disorders similar to elastic pseudo-xanthoma). Typically this condition is inherited as an autosomal recessive disease. Despite this, indications of disease are often observed even in the parents of a patient, due to the presence of slight abnormalities in coagulation. Genetic counseling should be offered to affected families, although prenatal genetic testing is generally not recommended. The administration of vitamin K during the third trimester of pregnancy can be useful to women at risk. The administration of vitamin K is the therapy of choice in the case of the symptomatic form of the combined deficit. Administration of plasma and prothrombin complex concentrates during surgery or severe bleeding episodes is helpful. An alternative therapeutic option in view of surgery and in the presence of serious bleeding is the combination of recombinant activated FVII (activated eptacog alfa) and vitamin K. The general prognosis is good, especially if the diagnosis is early and with effective therapy.



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Marfan syndrome is a systemic connective tissue disease characterized by the variable association of cardiovascular, musculoskeletal, ocular, and pulmonary symptoms. The estimated prevalence is 1/5,000, with no difference between the sexes. Symptoms can occur at all ages and vary considerably among affected people, even within the same family. Cardiovascular involvement is characterized by: 1) progressive dilation of the aorta, associated with an increased risk of aortic dissection. Aortic dilatation can result in insufficiency of the aortic valve; 2) mitral valve insufficiency, which can be complicated by arrhythmias, endocarditis or heart failure. The involvement of the skeleton is often the first sign of the disease and includes excessive length of the extremities, being overweight, arachnodactyly, hypermobility of the joints, scoliosis, and deformity of the chest or maxillary region. The ocular signs include detachment of the retina and dislocation of the lens. Eye complications can result in blindness. Skin signs (stretch marks) may be present, and the risk of respiratory complications is increased. In most cases, Marfan syndrome is caused by mutations in the FBN1 gene (15q21) which encodes fibrillin-1, an essential connective tissue protein. Some borderline clinical forms are due to mutations in the TGFBR2 gene, located on chromosome 3, which codes for a TGF-beta receptor. Transmission is autosomal dominant: it is sufficient to have a single copy of the gene mutated to manifest the condition. A pharmacological treatment has recently been proposed (with ACE inhibitors) which seems to give excellent results also in terms of prevention of complications.

Ehlers-Danlos syndrome (EDS) includes a heterogeneous group of hereditary connective tissue diseases, characterized by joint hyperclass, hyperelastic skin and tissue fragility. The classic type (which includes EDS types 1 and 2) is characterized by the following major diagnostic criteria: hyperextensibility of the skin, atrophic skin scars due to tissue fragility and joint hyper-class. Other minor symptoms are joint subluxations, muscle hypotonia and the presence of family history of the disease. The prevalence of the classic type is estimated at 1:30,000. In most cases, the transmission is autosomal dominant: it is sufficient to have a single copy of the gene mutated to manifest the condition.




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